Gabapentin Attenuates Ocular Inflammation: In vitro and In vivo Studies

Anfuso, Carmelina Daniela; Olivieri, Melania; Fidilio, Annamaria; Lupo, Gabriella; Rusciano, Dario; Pezzino, Salvatore; Gagliano, Caterina; Drago, Filippo; Bucolo, Claudio

doi:10.3389/fphar.2017.00173

Cited by 41 publications

(38 citation statements)

References 32 publications

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“…Our observations are in good agreement with the results obtained by Choi et al (2012), who demonstrated increased COX-2 expression in gingival fibroblasts treated with LPS [10]. Similar findings were obtained by Anfuso et al (2017) for rabbit corneal epithelial cells [11]. Taking into account the changes in NO and COX-2 levels caused by induction of the ocular surface cells with LPS, we may suppose that these compounds are not necessarily involved in triggering inflammation.…”

Section: Discussionsupporting

confidence: 93%

Reactivity of corneal and conjunctival epithelial cells to lipopolysaccharide (LPS) and/or irradiation with visible light in vitro

Paduch¹,

Matysik-Woźniak²,

Maciejewski³

et al. 2018

Ophthalmol J

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introduCtion. Visible light and inflammation caused by bacterial endotoxins strongly influence direct cell interactions and modulate the expression of selected factors, such as nitric oxide (NO) and cyclooxygenase-2 (COX-2). The aim of the study is to establish whether exposition of corneal or conjunctival epithelial cells to visible light and/ or LPS may change their viability, direct cellular interactions and expression of NO and COX-2. MateriaLs and Methods. In vitro cultured human corneal and conjunctival epithelial cells were used in the study. The following assays were performed: Neutral Red (NR) uptake, nitric oxide (NO) quantification by the Griess method, cytoskeletal F-actin organization by fluorescent staining, and COX-2 expression by immunofluorescence. resuLts. LPS reduced the viability of the cells, especially conjunctival epithelial cells. All cell stimulation variants tested (visible light and/or LPS treatment) led to decreased nitric oxide (NO) production both by corneal and conjunctival epithelial cells. No changes in cytoskeletal F-actin filaments were observed after the cells had been treated with light or the endotoxin. LPS slightly increased COX-2 expression, but light had no, or a slightly reducing, effect on the level of this enzyme. ConCLusions. Visible light and/or bacterial endotoxin (LPS) may, depending on the local microenvironmental conditions, cooperate or interfere with each other's activity in inducing ocular surface inflammation.

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Section: Discussionsupporting

confidence: 93%

Reactivity of corneal and conjunctival epithelial cells to lipopolysaccharide (LPS) and/or irradiation with visible light in vitro

Paduch¹,

Matysik-Woźniak²,

Maciejewski³

et al. 2018

Ophthalmol J

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“…H&E staining revealed marked inflammatory cell infiltration in the iris-ciliary body region and the posterior vitreous cavity 24 h after the intravitreal injection of LPS (Fig. 1b), and the mRNA levels of TNF-α, a well-known marker of ocular inflammation [23], were also significantly increased in the retina by LPS (Fig. 1c).…”

Section: Resultsmentioning

confidence: 99%

Lipocalin 2 Suppresses Ocular Inflammation by Inhibiting the Activation of NF-κβ Pathway in Endotoxin-Induced Uveitis

Tang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Lipocalin 2 (LCN2), an important mediator of a variety of cellular processes, is involved in regulating the inflammatory response, but its roles in different inflammatory diseases are controversial. Because the role of LCN2 in ocular inflammation has been unclear until now, we explored the function of LCN2 in lipopolysaccharide (LPS)-induced ocular inflammation in vivo and in vitro. Methods: Endotoxin-induced uveitis (EIU) was induced in male Sprague Dawley rats by the intravitreal injection of LPS. The expression and location of LCN2 in the retina were detected with western blotting and immunohistochemistry, respectively. We determined the clinical scores for anterior inflammation, quantified the infiltrated inflammatory cells, and measured the pro-inflammatory factors to determine the anti-inflammatory effects of LCN2 in EIU eyes. Cultured primary rat Müller cells were stimulated with LPS and the expression and secretion of LCN2 were measured with real-time PCR, western blotting, and an ELISA. After Müller cells were cotreated with LPS and LCN2 or PBS, the expression and secretion of TNF-α, IL-6, and MCP-1 were examined with realtime PCR, western blotting, and ELISAs. Western blotting and immunofluorescence were used to detect the phosphorylation and cellular distribution of nuclear factor kappaB (NF-κB) subunit p65. Results: In EIU, the expression of LCN2 was significantly upregulated in the retina, especially in the outer nuclear layer (mainly composed of Müller cells). LPS stimulation of cultured Müller cells also markedly elevated LCN2 expression. Intravitreal injection of LCN2 significantly reduced the clinical scores, inflammatory infiltration, and protein leakage in EIU, which correlated with the reduced levels of proinflammatory factors in the aqueous humor and retina. LCN2 treatment also reduced the expression and secretion of TNF-α, IL-6, and MCP-1 in LPS-stimulated Müller cells. LCN2 inhibited the inflammatory response by inhibiting the phosphorylation and translocation of NF-κB p65. Conclusions: LCN2 protects against ocular inflammation, at least in part, by negatively regulating the activation of the NF-κB signaling pathway. LCN2 may be a promising anti-inflammatory therapy for ocular diseases, such as uveitis.

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“…No. 539134) as described previously [13]. Briefly, cell monolayers were rinsed 3 times with cold PBS, and extracted for 30 min on ice.…”

Section: Ecm Proteins Analysis By Western Blottingmentioning

confidence: 99%

Atropine Differentially Modulates ECM Production by Ocular Fibroblasts, and Its Ocular Surface Toxicity Is Blunted by Colostrum

et al. 2020

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Background: The etiology and the mechanism behind atropine treatment of progressive myopia are still poorly understood. Our study addressed the role of scleral and choroidal fibroblasts in myopia development and atropine function. Methods: Fibroblasts treated in vitro with atropine or 7-methylxanthine were tested for ECM production by Western blotting. Corneal epithelial cells were treated with atropine in the presence or absence of colostrum or fucosyl-lactose, and cell survival was evaluated by the MTT metabolic test. Results: Atropine and 7-methyl-xanthine stimulated collagen I and fibronectin production in scleral fibroblasts, while they inhibited their production in choroidal fibroblasts. Four days of treatment with atropine of corneal epithelial cells significantly decreased cell viability, which could be prevented by the presence of colostrum or fucosyl-lactose. Conclusions: Our results show that atropine may function in different ways in different eye districts, strengthening the scleral ECM and increasing permeability in the choroid. The finding that colostrum or fucosyl-lactose attenuate the corneal epithelial toxicity after long-term atropine treatment suggests the possibility that both compounds can efficiently blunt its toxicity in children subjected to chronic atropine treatment.

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Gabapentin Attenuates Ocular Inflammation: In vitro and In vivo Studies

Cited by 41 publications

References 32 publications

Reactivity of corneal and conjunctival epithelial cells to lipopolysaccharide (LPS) and/or irradiation with visible light in vitro

Reactivity of corneal and conjunctival epithelial cells to lipopolysaccharide (LPS) and/or irradiation with visible light in vitro

Lipocalin 2 Suppresses Ocular Inflammation by Inhibiting the Activation of NF-κβ Pathway in Endotoxin-Induced Uveitis

Atropine Differentially Modulates ECM Production by Ocular Fibroblasts, and Its Ocular Surface Toxicity Is Blunted by Colostrum

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